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38 Cards in this Set
- Front
- Back
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What does arteriosclerosis mean? and what are the three types?
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"hardening of the arteries"
1. athersclerosis 2. arteriolosclerosis 3. Monckeberg medial calcific sclerosis |
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What is athersclerosis?
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intimal thickening & lipid deposition
elastic & large/medium-sized muscular arteries |
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What is arteriolosclerosis?
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non-atherosclerotic: small arteries & arterioles (hypertension)
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What is Monckeberg medial calcific sclerosis?
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calcification of media of muscular arteries
usually of no clinical significance |
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What are the three leading causes of death in the U.S.? (60% of all deaths)
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Heart Disease
Cancer Stroke |
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What are the major clinical outcomes in atherosclerosis?
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Heart Attack
Angina Stroke PVD |
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What are the differences in CAD, CHD, CVD and CHF?
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CAD/CHD: coronary --> angina & MI
CVD: broad --> includes HTN, stroke, defects, etc. CHF: failure; broad --> inability to properly supply blood |
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What has been the trend in deaths in the U.S. from CVD from 1900 to now?
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Dramatically increased up until ~1970, has since begun to decrease (primary prevention (lifestyle, htn mgmt) and secondary (better care/knowledge/technology))
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when does atherosclerosis start?
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childhood! (slowly progressive disease)
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what is a raised fibrofatty plaque consisting of a core of lipid & fibrous cap?
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atheroma (basic lesion in atherosclerosis development)
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What are the three "general" categories of atherosclerosis risks factors?
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1. non-modifiable
2. potentially controllable 3. lesser, uncertain, or unquantified |
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what are the three non-modifiable risk factors for atherosclerosis?
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1. age
2. male gender 3. family history/genetic abnormalities |
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What were the two seminal studies to identify potentially controllable atherosclerosis risk factors?
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Farmingham and MrFit
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what are the five potentially controllable atherosclerosis risk factors?
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1. hyperlipidemia*
2. hypertension 3. smoking 4. diabetes 5. c-reactive protein (new) -- inflammation |
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what are atherosclerotic plaques rich in?
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cholesterol and cholesterol esters derived from lipoproteins in the blood (linking atherosclerosis and hypercholesterolemia)
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which study showed an increased CHD mortality with increasing levels of cholesterol? and at what "level" did the increase occur most rapidly?
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MRFIT; >200 TC
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Despite a recommend TC of <200, how does the US compare to other countries?
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higher, where CHD is rare, TC avg. ~130-140
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How does the association of LDL compare to TC alone with CHD?
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LDL has greater association; current Optimal is <100 (lower than previous recommendation)
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what is the "optimal" LDL for those with CHD or CHD equivalent (what does CHD equivalent mean?)?
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<100; diabetes is the "equivalent" to CHD diagnosis
LDL goal increase |
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What are the Risk Factors in determining optimal LDL levels?
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1. smoking
2. HTN 3. Low HDL (<40) 4. FH of premature CHD 5. Age (>45 males, >55 females) |
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What is HDL involved in?
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"reverse cholesterol transport"
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What are desirable HDL levels?
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< 40 LOW
> 60 HIGH (protective) |
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Are triglycerides (TG) a risk factor for CHD?
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it is unclear
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The risk of CHD markedly increases when the ratio of TC/HDL exceeds what?
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>4.5
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what is the impact of mono-unsaturated fats on LDL and HDL?
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decrease LDL
increase HDL |
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what is the impact of poly-unsaturated fats on LDL and HDL?
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decrease LDL
& can decrease HDL |
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What effect does a low-fat dietary pattern have on CHD, stroke and total CVD?
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None! (decrease in the study was for all types of fat -- not just saturated)
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What are the two sources of cholesterol and what is the most common?
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exogenous (diet)
& endogenous -- most cholesterol is synthesized de novo (liver is major site of synthesis) |
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Is cholesterol soluble?
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No. Insoluble, requires special transport system (spherical LIPOPROTEINS)
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What is cholesterol used for?
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cell membranes, synthesis of bile acids, steroid hormone production
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what are exogenous dietary lipids packaged into for transport?
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chylomicrons (yummy chylomicrons)
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What is the endogenous pathway for cholesterol?
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VLDL (from liver, TG rich) --> IDL --> LDL
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What are the two mechanisms LDL is removed from the plasma?
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1. LDL receptor pathway (~70% by the liver)
2. Scavenger receptor pathway (monocytes and macrophages) |
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How is oxidized or modified LDL taken up? (by what)? why is this important in atherosclerosis?
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Scavenger receptor pathway (monocytes and macrophages) --> more important than LDL receptors in atherosclerosis (oxidized LDLs cannot be taken up by liver); in circulation = developing atherosclerosis
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What happens to IDL in FH (familial hypercholesterolemia)?
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defect in LDL receptors, IDL cannot be taken up --> converted to LDL --> not taken up --> high LDL in plasma
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what is a squishy collection of cholesterol, appearing on the skin?
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Xanthoma (very high LDLs)
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What is the inheritance pattern of FH? and prevalence?
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AD; 1:500
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what is the difference between heterozygote and homozygote FH?
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hetero: reduced LDL receptors --> TC: 250-500, premature MI
homo: ABSENT LDL receptors --> TC: 600-1000; CAD may die before 15-20 |
